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The Pineal Gland
Published in Nate F. Cardarelli, The Thymus in Health and Senescence, 2019
Campbell first drew attention to the similarity of cells in the human retina and pineal gland.219 In 1977 Kurumado and Mori noted that the human fetal pineal has many tightly packed cuboidal cells with cilia, which is characteristic of the photoreceptors of the adult retina.220 In the rare congenital disease Reece’s syndrome, patients have multiple abnormalities. Retinal dysplasia is marked. In two cases reported by Mori and Okeda, one had a marked hypoplasia of the pineal, and in the other no pineal gland could be located.221 It has also been noted that human pineoblastomas will occasionally differentiate into retinoblastomas.222 Although evidence is sparse indeed as regards human beings, there are indications, as mentioned previously, of retinal and pineal similarities.
Special Senses
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Kenneth A. Schafer, Oliver C. Turner, Richard A. Altschuler
Alterations involving photoreceptors include dysplasia, dystrophy, and degeneration. The term “retinal dysplasia” is used to describe focal or multifocal disorganization of the sensory retina due to faulty development and is usually characterized by retinal rosettes, abnormal alignment of photoreceptor cells, and possible degeneration. Spontaneous retinal dysplasia occurs in many laboratory animals, especially rats and rabbits (Rubin 1974). In the rat, retinal dysplasia generally consists of unilateral, linear areas of thinning or loss of the outer layers of the sensory retina, with occasional direct abutment of the INL to the choroid or sclera (Hubert et al. 1994; Kuno et al. 1991; Lin and Essner 1987; Schardein et al. 1975; Taradach and Greaves 1984; Taradach et al. 1981). The finding may occur more frequently in males with an increased incidence with age. One example is referred to as linear retinopathy (Figure 23.3d). Retinal dysplasia may also occur as a finding associated with toxicity (e.g., cytosine in rat pups) (Percy and Danylchuk 1977).
Bilateral Central Retinal Vein Occlusion in a Neonate
Published in Ocular Immunology and Inflammation, 2023
Piyush Kohli, Haemoglobin Parida, Renu P. Rajan, Naresh Babu Kannan
At presentation to our hospital (6 weeks age), ocular examination showed poorly dilating pupil, a hazy media, disc edema, and hemorrhage, dilated retinal veins, perivascular exudation, intraretinal hemorrhages in all four quadrants radiating from the optic nerve to the ora serrata, pallid retina, and cystoid macular edema (CME) in both the eyes. All the hemorrhages were intraretinal. There was no evidence of any trauma, ROP, Roth spots, viral retinitis, or retinal dysplasia (Figure 1). The infant was afebrile and systemically stable. Blood investigations showed hemoglobin 11.6 g/dL and platelet count 298000/μL. Serological tests for TORCH (Toxoplasmosis, Rubella, Cytomegalovirus, and Herpes) were negative. He was presumptively diagnosed as bilateral inflammatory CRVO with CME secondary to septicemia and thrombocytopenia.
Keratoconus in a child with partial trisomy 13
Published in Ophthalmic Genetics, 2021
Julia Ernst, Amgad Eldib, Hannah L. Scanga, Ken K. Nischal
Patau syndrome (complete trisomy 13) is a rare abnormality that manifests as a triad of microphthalmia, cleft lip and palate, and polydactyly. Most patients present at birth with severe malformations leading to early death. However, in incomplete trisomy 13, patients may show a few dysmorphic features and relatively normal development (1). Patients usually require multiple medical treatments by different specialists. The frequently described ocular manifestations are microphthalmia, uveal tract colobomas, retinal dysplasia, persistence and hyperplasia of the primary vitreous body, cataract and lens luxation (2). To our knowledge, keratoconus has not been reported in a patient with complete, mosaic or partial trisomy 13. Keratoconus is characterized by progressive thinning and cone-shaped protrusion of the cornea, leading to progressive visual impairment (3). It is mostly a sporadic disorder with major risk factors including eye rubbing, atopy, systemic disorders and contact lens use. Clinical studies suggest genetic components in its etiology, but the contributing alleles remain elusive (3).
Novel ocular findings in oculodentodigital dysplasia (ODDD): a case report and literature review
Published in Ophthalmic Genetics, 2019
Zhirong Wang, Limei Sun, Panfeng Wang, Chonglin Chen, Aiyuan Zhang, Weiqing Wang, Xiaoyan Ding
Our patient had structural and functional retinal impairment, as verified with both OCT and ERG evaluations. The preserved inner retinal layer in macular area was recently reported in several diseases, including retinopathy of prematurity (ROP), stickler syndrome, and familial exudative vitreoretinopathy (FEVR) (31–33). Thus, we suggest that retinal impairment might be underestimated in previous reports since optic nerve and retinal dysplasia had not been emphasized as ocular manifestations ODDD. Finally, the fundus phenotype in this case differs from that in the previous reports, which indicated that Cx43 mutations could cause various ocular and systemic phenotypes.